Evidence map›Paper›PMID 39681572›Full record

ArticleScientific reports2024

Renal phenotyping in a hypomorphic murine model of propionic aciduria reveals common pathomechanisms in organic acidurias.

Anke Schumann, Ainhoa Martinez-Pizarro, Eva Richard, Christoph Schell, Anna Laura Kössinger, Karina A Zeyer, Stefan Tholen, Oliver Schilling, Michael Barry, Björn Neubauer and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Scientific reports, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Review
  2. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

14 authors.

Anke SchumannDepartment of General Paediatrics, Adolescent Medicine and Neonatology, Faculty of Medicine, Medical Center, University of Freiburg, Breisacherstr. 62, 79106, Freiburg, Germany. anke.schumann@uniklinik-freiburg.de.
Ainhoa Martinez-PizarroCentro de Biología Molecular Severo Ochoa, UAM-CSIC, CIBERER, IdiPaz, IUBM, Universidad Autónoma de Madrid, Madrid, Spain.
Eva RichardCentro de Biología Molecular Severo Ochoa, UAM-CSIC, CIBERER, IdiPaz, IUBM, Universidad Autónoma de Madrid, Madrid, Spain.
Christoph SchellFaculty of Medicine, Medical Center, University of Freiburg, Institute for Surgical Pathology, Freiburg, Germany.
Anna Laura KössingerFaculty of Medicine, Medical Center, University of Freiburg, Institute for Surgical Pathology, Freiburg, Germany.
Karina A ZeyerDepartment of General Paediatrics, Adolescent Medicine and Neonatology, Faculty of Medicine, Medical Center, University of Freiburg, Breisacherstr. 62, 79106, Freiburg, Germany.
Stefan TholenFaculty of Medicine, Medical Center, University of Freiburg, Institute for Surgical Pathology, Freiburg, Germany.
Oliver SchillingFaculty of Medicine, Medical Center, University of Freiburg, Institute for Surgical Pathology, Freiburg, Germany.
Michael BarryDepartment of Medicine, Division of Infectious Diseases, Mayo Clinic, Rochester, MN, 55905, USA.
Björn NeubauerDepartment of Medicine IV - Nephrology and Primary Care, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany.
Michael KöttgenDepartment of Medicine IV - Nephrology and Primary Care, Faculty of Medicine and Medical Center, University of Freiburg, Freiburg, Germany.
Luciana HannibalDepartment of General Paediatrics, Adolescent Medicine and Neonatology, Laboratory of Clinical Biochemistry and Metabolism, Faculty of Medicine, Medical Center, University of Freiburg, Freiburg, Germany.
Lourdes R DesviatCentro de Biología Molecular Severo Ochoa, UAM-CSIC, CIBERER, IdiPaz, IUBM, Universidad Autónoma de Madrid, Madrid, Spain.
Ute SpiekerkötterDepartment of General Paediatrics, Adolescent Medicine and Neonatology, Faculty of Medicine, Medical Center, University of Freiburg, Breisacherstr. 62, 79106, Freiburg, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Mutations in the mitochondrial enzyme propionyl-CoA carboxylase (PCC) cause propionic aciduria (PA). Chronic kidney disease (CKD) is a known long-term complication. However, good metabolic control and standard therapy fail to prevent CKD. The pathophysiological mechanisms of CKD are unclear. We investigated the renal phenotype of a hypomorphic murine PA model (Pcca

Indexed as

Disease Models, AnimalKidneyMethylmalonyl-CoA DecarboxylaseMitochondriaPhenotypePropionic AcidemiaAnimalsCitric Acid CycleMiceMitochondrial DynamicsMitophagyOxidative StressPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaRenal Insufficiency, ChronicMethylmalonyl-CoA DecarboxylasePeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaChronic kidney diseaseMitochondrial dysfunctionMitochondrial energy metabolismMitochondrial fissionMitochondrial homeostasisMitochondrial quality controlPropionic aciduria

Identifiers

PMID39681572
PMCPMC11649940

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.